Peripheral chemoreceptor control of exercise hyperpnea in humans.

Medicine & Science in Sports & Exercise:

WHIPP, B. J. Peripheral chemoreceptor control of exercise hyperpnea in humans. Med. Sci. Sports Exerc., Vol. 26, No. 3, pp. 337-347, 1994. Estimates of the proportional contribution of the peripheral chemoreceptors (i.e., the carotid bodies) to human ventilatory control during moderate exercise (i.e., below the lactate threshold, [middle dot]1) suggest that they: (a) exert no discernible influence on the initial (usually rapid) phase I component; (b) provide significant modulation of the slower, exponential phase II dynamics, therefore contributing to the tightness of arterial PCO2 regulation and the magnitude of the transient hypoxemia in this phase; and (c) account for ~20% of the steady-state phase III drive, which can rise to over 50% in hypoxia (PaO2 ~50 mm Hg). Above [theta]1, the carotid bodies constrain the transient fall in arterial pH by mediating much (but not all) of the compensatory hyperventilation for the metabolic acidemia. The carotid body contribution above [theta]1, estimated by Dejours O2 testing, is not appreciably different from subthreshold estimates, suggesting that: (a) the respiratory alkalosis in blood and cerebrospinal fluid resulting from the hyperventilation may suppress carotid chemonsitivity; (b) an artifact resulting from secondary hyperoxia-induced stimulation of central chemoreceptors may lead to underestimation of the carotid body contribution; or (c) the carotid bodies may not be entirely "silenced" by hyperoxia during a metabolic acidemia.

(C)1994The American College of Sports Medicine